Showing papers on "Rapid eye movement sleep published in 2020"
TL;DR: A more sophisticated research framework for sleep-deprivation procedures that could benefit from recent progress in biotechnological tools for precise neuromodulation, such as chemogenetics and optogenetics, as well as improved automated real-time sleep-scoring algorithms are proposed.
Abstract: Sleep is highly conserved across evolution, suggesting vital biological functions that are yet to be fully understood. Animals and humans experiencing partial sleep restriction usually exhibit detrimental physiological responses, while total and prolonged sleep loss could lead to death. The perturbation of sleep homeostasis is usually accompanied by an increase in hypothalamic-pituitary-adrenal (HPA) axis activity, leading to a rise in circulating levels of stress hormones (e.g. cortisol in humans, corticosterone in rodents). Such hormones follow a circadian release pattern under undisturbed conditions and participate in the regulation of sleep. The investigation of the consequences of sleep deprivation, from molecular changes to behavioural alterations, has been used to study the fundamental functions of sleep. However, the reciprocal relationship between sleep and the activity of the HPA axis is problematic when investigating sleep using traditional sleep-deprivation protocols that can induce stress per se. This is especially true in studies using rodents in which sleep deprivation is achieved by exogenous, and potentially stressful, sensory-motor stimulations that can undoubtedly confuse their conclusions. While more research is needed to explore the mechanisms underlying sleep loss and health, avoiding stress as a confounding factor in sleep-deprivation studies is therefore crucial. This review examines the evidence of the intricate links between sleep and stress in the context of experimental sleep deprivation, and proposes a more sophisticated research framework for sleep-deprivation procedures that could benefit from recent progress in biotechnological tools for precise neuromodulation, such as chemogenetics and optogenetics, as well as improved automated real-time sleep-scoring algorithms.
88 citations
TL;DR: Melatonin may reduce REM‐sleep behavior disorder (RBD) symptoms in Parkinson's disease (PD), though robust clinical trials are lacking.
Abstract: Background Melatonin may reduce REM-sleep behavior disorder (RBD) symptoms in Parkinson's disease (PD), though robust clinical trials are lacking. Objective To assess the efficacy of prolonged-release (PR) melatonin for RBD in PD. Methods Randomized, double-blind, placebo-controlled, parallel-group trial with an 8-week intervention and 4-week observation pre- and postintervention (ACTRN12613000648729). Thirty PD patients with rapid eye movement sleep behavior disorder were randomized to 4 mg of prolonged-release melatonin (Circadin) or matched placebo, ingested orally once-daily before bedtime. Primary outcome was the aggregate of rapid eye movement sleep behavior disorder incidents averaged over weeks 5 to 8 of treatment captured by a weekly diary. Data were included in a mixed-model analysis of variance (n = 15 per group). Results No differences between groups at the primary endpoint (3.4 events/week melatonin vs. 3.6 placebo; difference, 0.2; 95% confidence interval = -3.2 to 3.6; P = 0.92). Adverse events included mild headaches, fatigue, and morning sleepiness (n = 4 melatonin; n = 5 placebo). Conclusion Prolonged-release melatonin 4 mg did not reduce rapid eye movement sleep behavior disorder in PD. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
78 citations
TL;DR: This study suggests that PD patients have poor sleep quality and quantity, and identifies factors that contributed to heterogeneity between studies.
65 citations
TL;DR: Findings show that compared to healthy controls, those with MCI have pronounced changes in sleep macro-architecture with greater wake after sleep onset, reduced total sleep time, lower sleep efficiency, longer sleep onset latency, longer rapid eye movement sleep (REM) latency, reduced REM sleep, greater N1 sleep, and worse severity of hypoxemia.
56 citations
TL;DR: The clinical characteristics, diagnosis, and possible mechanisms of RBD in neurogenerative diseases, including Alzheimer's disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), etc. are updated.
Abstract: Rapid eye movement sleep behavior disorder (RBD) is a sleep behavior disorder characterized by abnormal behaviors and loss of muscle atonia during rapid eye movement (REM) sleep. RBD is generally considered to be associated with synucleinopathies, such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), and usually precedes years before the first symptom of these diseases. It is believed that RBD predicts the neurodegeneration in synucleinopathy. However, increasing evidences have shown that RBD is also found in non-synucleinopathy neurodegenerative diseases, including Alzheimer's disease (AD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), etc. Sleep disturbance such as RBD may be an early sign of neurodegeneration in these diseases, and also serve as an assessment of cognitive impairments. In this review, we updated the clinical characteristics, diagnosis, and possible mechanisms of RBD in neurogenerative diseases. A better understanding of RBD in these neurogenerative diseases will provide biomarkers and novel therapeutics for the early diagnosis and treatment of the diseases.
45 citations
TL;DR: Sleep analysis based on electroencephalogram and electromyogram recordings revealed that AIMD mice spent significantly less time in non-rapid eye movement sleep (NREMS) during the light phase while spending more time in NREMS and rapid eye movementSleep (REMS), during the dark phase.
Abstract: Dysbiosis of the gut microbiota affects physiological processes, including brain functions, by altering the intestinal metabolism. Here we examined the effects of the gut microbiota on sleep/wake regulation. C57BL/6 male mice were treated with broad-spectrum antibiotics for 4 weeks to deplete their gut microbiota. Metabolome profiling of cecal contents in antibiotic-induced microbiota-depleted (AIMD) and control mice showed significant variations in the metabolism of amino acids and vitamins related to neurotransmission, including depletion of serotonin and vitamin B6, in the AIMD mice. Sleep analysis based on electroencephalogram and electromyogram recordings revealed that AIMD mice spent significantly less time in non-rapid eye movement sleep (NREMS) during the light phase while spending more time in NREMS and rapid eye movement sleep (REMS) during the dark phase. The number of REMS episodes seen in AIMD mice increased during both light and dark phases, and this was accompanied by frequent transitions from NREMS to REMS. In addition, the theta power density during REMS was lower in AIMD mice during the light phase compared with that in the controls. Consequently, the gut microbiota is suggested to affect the sleep/wake architecture by altering the intestinal balance of neurotransmitters.
44 citations
TL;DR: This study assesses regional variations of electroencephalographic sleep activity and creates the first atlas of human sleep using recordings from the first sleep cycle.
Abstract: Objective Regional variations in oscillatory activity during human sleep remain unknown. Using the unique ability of intracranial electroencephalography to study in situ brain physiology, this study assesses regional variations of electroencephalographic sleep activity and creates the first atlas of human sleep using recordings from the first sleep cycle. Methods Intracerebral electroencephalographic recordings with channels displaying physiological activity from nonlesional tissue were selected from 91 patients of 3 tertiary epilepsy centers. Sections during non-rapid eye movement sleep (stages N2 and N3) and rapid eye movement sleep (stage R) were selected from the first sleep cycle for oscillatory and nonoscillatory signal analysis. Results of 1,468 channels were grouped into 38 regions covering all cortical areas. Results We found regional differences in the distribution of sleep transients and spectral content during all sleep stages. There was a caudorostral gradient, with more slow frequencies and fewer spindles in temporoparieto-occipital than in frontal cortex. Moreover, deep-seated structures showed spectral peaks differing from the baseline electroencephalogram. The regions with >60% of channels presenting significant rhythmic activity were either mesial or temporal basal structures that contribute minimally to the scalp electroencephalogram. Finally, during deeper sleep stages, electroencephalographic analysis revealed a more homogeneous spatial distribution, with increased coupling between high and low frequencies. Interpretation This study provides a better understanding of the regional variability of sleep, and establishes a baseline for human sleep in all cortical regions during the first sleep cycle. Furthermore, the open-access atlas will be a unique resource for research (https://mni-open-ieegatlas. Research mcgill.ca). ANN NEUROL 2020;87:289-301.
41 citations
TL;DR: Reduced percentage REM sleep was associated with greater risk of all-cause, cardiovascular, and other noncancer-related mortality in 2 independent cohorts and a random forest model identified REM sleep as the most important sleep stage associated with survival.
Abstract: Importance Rapid eye movement (REM) sleep has been linked with health outcomes, but little is known about the relationship between REM sleep and mortality. Objective To investigate whether REM sleep is associated with greater risk of mortality in 2 independent cohorts and to explore whether another sleep stage could be driving the findings. Design, Setting, and Participants This multicenter population-based cross-sectional study used data from the Outcomes of Sleep Disorders in Older Men (MrOS) Sleep Study and Wisconsin Sleep Cohort (WSC). MrOS participants were recruited from December 2003 to March 2005, and WSC began in 1988. MrOS and WSC participants who had REM sleep and mortality data were included. Analysis began May 2018 and ended December 2019. Main Outcomes and Measures All-cause and cause-specific mortality confirmed with death certificates. Results The MrOS cohort included 2675 individuals (2675 men [100%]; mean [SD] age, 76.3 [5.5] years) and was followed up for a median (interquartile range) of 12.1 (7.8-13.2) years. The WSC cohort included 1386 individuals (753 men [54.3%]; mean [SD] age, 51.5 [8.5] years) and was followed up for a median (interquartile range) of 20.8 (17.9-22.4) years. MrOS participants had a 13% higher mortality rate for every 5% reduction in REM sleep (percentage REM sleep SD = 6.6%) after adjusting for multiple demographic, sleep, and health covariates (age-adjusted hazard ratio, 1.12; fully adjusted hazard ratio, 1.13; 95% CI, 1.08-1.19). Results were similar for cardiovascular and other causes of death. Possible threshold effects were seen on the Kaplan-Meier curves, particularly for cancer; individuals with less than 15% REM sleep had a higher mortality rate compared with individuals with 15% or more for each mortality outcome with odds ratios ranging from 1.20 to 1.35. Findings were replicated in the WSC cohort despite younger age, inclusion of women, and longer follow-up (hazard ratio, 1.17; 95% CI, 1.03-1.34). A random forest model identified REM sleep as the most important sleep stage associated with survival. Conclusions and Relevance Decreased percentage REM sleep was associated with greater risk of all-cause, cardiovascular, and other noncancer-related mortality in 2 independent cohorts.
41 citations
TL;DR: By long-term recording of MS cholinergic neurons, it is found that they show a theta state-related firing pattern and optogenetically activating these neurons shows little effect on theta rhythm in the hippocampus, and activating them during slow-wave sleep could suppress hippocampal ripple oscillations.
Abstract: The septo-hippocampal cholinergic system is critical for hippocampal learning and memory. However, a quantitative description of the in vivo firing patterns and physiological function of medial septal (MS) cholinergic neurons is still missing. In this study, we combined optogenetics with multichannel in vivo recording and recorded MS cholinergic neuron firings in freely behaving male mice for 5.5-72 h. We found that their firing activities were highly correlated with hippocampal theta states. MS cholinergic neurons were highly active during theta-dominant epochs, such as active exploration and rapid eye movement sleep, but almost silent during non-theta epochs, such as slow-wave sleep (SWS). Interestingly, optogenetic activation of these MS cholinergic neurons during SWS suppressed CA1 ripple oscillations. This suppression could be rescued by muscarinic M2 or M4 receptor antagonists. These results suggest the following important physiological function of MS cholinergic neurons: maintaining high hippocampal acetylcholine level by persistent firing during theta epochs, consequently suppressing ripples and allowing theta oscillations to dominate.SIGNIFICANCE STATEMENT The major source of acetylcholine in the hippocampus comes from the medial septum. Early experiments found that lesions to the MS result in the disappearance of hippocampal theta oscillation, which leads to speculation that the septo-hippocampal cholinergic projection contributing to theta oscillation. In this article, by long-term recording of MS cholinergic neurons, we found that they show a theta state-related firing pattern. However, optogenetically activating these neurons shows little effect on theta rhythm in the hippocampus. Instead, we found that activating MS cholinergic neurons during slow-wave sleep could suppress hippocampal ripple oscillations. This suppression is mediated by muscarinic M2 and M4 receptors.
38 citations
TL;DR: The classical TRN-TC-CT spindle pathway is extended to include non-sensory thalamic nuclei and implicate spindles in the onset of REM sleep, finding that spindle rate significantly increases before the start of rapid eye movement (REM) sleep, but not wakefulness.
Abstract: Sleep spindle generation classically relies on an interplay between the thalamic reticular nucleus (TRN), thalamo-cortical (TC) relay cells and cortico-thalamic (CT) feedback during non-rapid eye movement (NREM) sleep. Spindles are hypothesized to stabilize sleep, gate sensory processing and consolidate memory. However, the contribution of non-sensory thalamic nuclei in spindle generation and the role of spindles in sleep-state regulation remain unclear. Using multisite thalamic and cortical LFP/unit recordings in freely behaving mice, we show that spike-field coupling within centromedial and anterodorsal (AD) thalamic nuclei is as strong as for TRN during detected spindles. We found that spindle rate significantly increases before the onset of rapid eye movement (REM) sleep, but not wakefulness. The latter observation is consistent with our finding that enhancing spontaneous activity of TRN cells or TRN-AD projections using optogenetics increase spindle rate and transitions to REM sleep. Together, our results extend the classical TRN-TC-CT spindle pathway to include non-sensory thalamic nuclei and implicate spindles in the onset of REM sleep.
35 citations
TL;DR: This study quantitatively evaluate iron content in idiopathic rapid eye movement sleep behavior disorder patients using quantitative susceptibility mapping and to examine the potential of this technique to identify the prodromal stage of α‐synucleinopathies.
Abstract: BACKGROUND Idiopathic rapid eye movement sleep behavior disorder is an early sign of neurodegenerative disease. This study aimed to quantitatively evaluate iron content in idiopathic rapid eye movement sleep behavior disorder patients using quantitative susceptibility mapping and to examine the potential of this technique to identify the prodromal stage of α-synucleinopathies. METHODS Twenty-five idiopathic rapid eye movement sleep behavior disorder patients, 32 Parkinson's disease patients, and 50 healthy controls underwent quantitative susceptibility mapping. The mean magnetic susceptibility values within the bilateral substantia nigra, globus pallidus, red nucleus, head of the caudate nucleus, and putamen were calculated and compared among groups. The relationships between the values and the clinical features of idiopathic rapid eye movement sleep behavior disorder and Parkinson's disease were measured using correlation analysis. RESULTS Idiopathic rapid eye movement sleep behavior disorder patients had elevated iron in the bilateral substantia nigra compared with healthy controls. Parkinson's disease patients had increased iron in the bilateral substantia nigra, globus pallidus, and left red nucleus compared with healthy controls and had elevated iron levels in the bilateral substantia nigra compared with idiopathic rapid eye movement sleep behavior disorder patients. Mean magnetic susceptibility values were positively correlated with disease duration in the left substantia nigra in idiopathic rapid eye movement sleep behavior disorder patients. CONCLUSIONS Quantitative susceptibility mapping can detect increased iron in the substantia nigra in idiopathic rapid eye movement sleep behavior disorder, which becomes more significant as the disorder progresses. This technique has the potential to be an early objective neuroimaging marker for detecting α-synucleinopathies. © 2019 International Parkinson and Movement Disorder Society.
TL;DR: These common sleep issues encountered in Parkinson's disease are reviewed and can significantly reduce sleep quantity, sleep quality, or quality of life for patients and caretakers.
TL;DR: Evidence is provided that elevated stress at encoding, and accompanying changes in neuromodulators such as cortisol, may interact with theta activity during REM sleep to promote selective consolidation of emotional information.
Abstract: Sleep and stress independently enhance emotional memory consolidation. In particular, theta oscillations (4-7 Hz) during rapid eye movement (REM) sleep increase coherence in an emotional memory network (i.e., hippocampus, amygdala, and prefrontal cortex) and enhance emotional memory. However, little is known about how stress during learning might interact with subsequent REM theta activity to affect emotional memory. In the current study, we examined whether the relationship between REM theta activity and emotional memory differs as a function of pre-encoding stress exposure and reactivity. Participants underwent a psychosocial stressor (the Trier Social Stress Task; n = 32) or a comparable control task (n = 32) prior to encoding. Task-evoked cortisol reactivity was assessed by salivary cortisol rise from pre- to post-stressor, and participants in the stress condition were additionally categorized as high or low cortisol responders via a median split. During incidental encoding, participants studied 150 line drawings of negative, neutral, and positive images, followed by the complete color photo. All participants then slept overnight in the lab with polysomnographic recording. The next day, they were given a surprise recognition memory task. Results showed that memory was better for emotional relative to neutral information. Critically, these findings were observed only in the stress condition. No emotional memory benefit was observed in the control condition. In stressed participants, REM theta power significantly predicted memory for emotional information, specifically for positive items. This relationship was observed only in high cortisol responders. For low responders and controls, there was no relationship between REM theta and memory of any valence. These findings provide evidence that elevated stress at encoding, and accompanying changes in neuromodulators such as cortisol, may interact with theta activity during REM sleep to promote selective consolidation of emotional information.
TL;DR: It is confirmed that sleep bruxism does not significantly affect sleep duration, efficiency and continuity (in terms of sleep–wake cycles), and those with bruXism present more frequent episodes during all stages of sleep.
Abstract: The aim of the study was to assess sleep structure, phenotypes related to bruxism activity and basic respiratory parameters among a large group of participants with sleep bruxism and without obstructive sleep apnea. Adult participants with clinical suspicion of sleep bruxism and with no other significant medical history were recruited. Video-polysomnography was performed to detect masseter muscles activity. Polysomnographic scoring was performed according to the American Academy of Sleep Medicine Criteria. Finally, 146 participants were included. The participants were divided into three subgroups: severe, mild and no sleep bruxism. There were no differences in total sleep time, sleep latency, sleep efficiency, wake duration after sleep onset, rapid eye movement, and measured respiratory parameters. The severity of sleep bruxism contributed to the increased intensity of all sleep bruxism phenotypes in almost all sleep stages, apart from tonic and mixed activity in non-rapid eye movement stage 3 sleep (slow-wave sleep). Those with bruxism spent more time in rapid eye movement sleep compared to controls; there were no differences in non-rapid eye movement sleep stages. The results confirmed that sleep bruxism does not significantly affect sleep duration, efficiency and continuity (in terms of sleep-wake cycles). Sleep bruxism contributes to a higher percentage of rapid eye movement sleep in the total sleep time. Those with bruxism present more frequent episodes during all stages of sleep; however, in the case of slow-wave sleep, tonic and mixed activity observed in participants with sleep bruxism are comparable to those of healthy people.
TL;DR: Circadian advancement and alterations to the timing of sleep and REM onset are evident in older people with lifetime major depression, despite having only mild residual symptoms.
Abstract: Depression is common in older people and is associated with underlying brain change increasing the risk of dementia. Sleep disturbance is frequently reported by those with lifetime depression, however whether circadian misalignment also exists is unclear. We aimed to examine circadian rhythms and sleep associations in older patients with and without lifetime depression. Thirty-four older people meeting DSM-IV criteria for lifetime major depression (mean age = 63.9 years), and 30 healthy controls (mean age = 65.7 years) were recruited. Participants underwent 2-weeks of actigraphy followed by a 3-night protocol including dim light melatonin onset (DLMO) assessment and overnight polysomnography (PSG) for sleep architecture. DLMO and phase angle of entrainment were computed. Compared to controls, participants with depression had a significantly longer phase angle of entrainment (6.82 h ± 1.45 vs. 5.87 h ± 1.60, p = 0.02, Cohens-d = 0.62). A small to moderate yet non-significant difference in DLMO times, with earlier DLMO (34 ± 27 min) observed in depression (20:36 ± 1:48 vs. 21:10 ± 1:48, p = 0.22, Cohens-d = 0.32). Individuals with depression had longer sleep latency and latency to rapid eye movement sleep than controls (all p < 0.05). Circadian advancement and alterations to the timing of sleep and REM onset are evident in older people with lifetime major depression, despite having only mild residual symptoms. Further research examining the prognostic significance of these changes is warranted as well as chronotherapeutic treatment studies.
TL;DR: It was showed that a large proportion of PD patients suffer from multiple comorbid sleep disorders, which greatly decreases the quality of life in PD patients and is partially mediated by motor complications.
Abstract: Sleep disorders are common non-motor symptoms in patients with Parkinson's disease (PD). The characteristics and impact of multiple comorbid sleep disorders remain to be elucidated. Our goal was to investigate the characteristics of various sleep disorder comorbidities, and their association with motor complications and the impact on the quality of life in PD patients. In this multicenter, observational, cross-sectional study, data concerning the clinical characteristics of complicated sleep disorders were collected from PD patients treated at 40 different hospitals in Shanghai. Sleep disorders were evaluated using the PD Sleep Scale-2, Epworth Sleepiness Scale, Rapid Eye Movement Sleep Behavior Disorder Questionnaire-Hong Kong, and the International Restless Legs Scale. Among the 1006 subjects evaluated, 77.53% exhibited signs of sleep disorders, and most had multiple sleep disorders (n = 502, 49.9%). A smaller percentage of patients with sleep disorders had a single disorder (n = 278, 27.6%). Furthermore, an increased number of sleep disorders, including nighttime problems, excessive daytime sleepiness, rapid eye movement sleep behavior disorder, and restless legs syndrome was a significant contributor to a poor quality of life (β = 4.33, CI: 3.33-5.33, P for trend <0.001), even when controlling for multiple factors. Moreover, motor complications partially mediated this relationship (indirect effect: β = 0.355, 95% boot CI: 0.134, 0.652).Our study showed that a large proportion of PD patients suffer from multiple comorbid sleep disorders, which greatly decreases the quality of life in PD patients and is partially mediated by motor complications.
TL;DR: SA, the only application offering the possibility of an epoch‐by‐epoch analysis, showed higher accuracy than the other apps in comparison with polysomnography, but it still shows some limitations, particularly regarding wake and deep sleep detection.
Abstract: An increasing number of sleep applications are currently available and are being widely used for in-home sleep tracking. The present study assessed four smartphone applications (Sleep Cycle-Accelerometer, SCa; Sleep Cycle-Microphone, SCm; Sense, Se; Smart Alarm, SA) designed for sleep-wake detection through sound and movement sensors, by comparing their performance with polysomnography. Twenty-one healthy participants (six males, 15 females) used the four sleep applications running on iPhone (provided by the experimenter) simultaneously with portable polysomnography recording at home, while sleeping alone for two consecutive nights. Whereas all apps showed a significant correlation with polysomnography-time in bed, only SA offered significant correlations for sleep efficacy. Furthermore, SA seemed to be quite effective in reliable detection of total sleep time and also light sleep; however, it underestimated wake and partially overestimated deep sleep. None of the apps resulted capable of detecting and scoring rapid eye movement sleep. To sum up, SC (functioning through both accelerometer and microphone) and Se did not result sufficiently reliable in sleep-wake detection compared with polysomnography. SA, the only application offering the possibility of an epoch-by-epoch analysis, showed higher accuracy than the other apps in comparison with polysomnography, but it still shows some limitations, particularly regarding wake and deep sleep detection. Developing scoring algorithms specific for smartphone sleep detection and adding external sensors to record other physiological parameters may overcome the present limits of sleep tracking through smart phone apps.
TL;DR: In this paper, the authors reviewed available evidence on the effects of therapies for sleep disorders on neuropsychiatric conditions and also secondarily considered the impacts of these therapies on sleep, identifying gaps in current research, to determine the extent to which the cross-therapeutic effects of these treatments help to elucidate therapeutic or pathological mechanisms, and to assist clinicians in optimizing therapeutic choice in patients with sleep disorders.
TL;DR: Thermoregulatory dysfunction is implicate as a potential early biomarker for development of rapid eye movement sleep behaviour disorder‐associated neurodegeneration, and subpopulations with differing pathological underpinnings might exist in Parkinson’s disease.
Abstract: The vast majority of patients with idiopathic rapid eye movement sleep behaviour disorder will develop a neurodegenerative α-synuclein-related condition, such as Parkinson's disease or dementia with Lewy bodies. The pathology underlying dream enactment overlaps anatomically with the brainstem regions that regulate circadian core body temperature. Previously, nocturnal core body temperature regulation has been shown to be impaired in Parkinson's disease. However, no study to date has investigated nocturnal core body temperature changes in patients with idiopathic rapid eye movement sleep behaviour disorder, which may prove to be an early objective biomarker for α-synucleinopathies. Ten healthy controls, 15 patients with idiopathic rapid eye movement sleep behaviour disorder, 31 patients with Parkinson's disease and six patients with dementia with Lewy bodies underwent clinical assessment and nocturnal polysomnography with core body temperature monitoring. A validated cosinor method was utilised for core body temperature analysis. No differences in mesor, nadir or time of nadir were observed between groups. However, when compared with healthy controls, the amplitude of the nocturnal core body temperature (mesor minus nadir) was significantly reduced in patients with idiopathic rapid eye movement sleep behaviour disorder, Parkinson's disease with concurrent rapid eye movement sleep behaviour disorder and dementia with Lewy bodies (p < 0.001, p = 0.043 and p = 0.017, respectively). Importantly, this relationship was not seen in those patients with Parkinson's disease without rapid eye movement sleep behaviour disorder. In addition, there was a significant negative correlation between amplitude of the core body temperature and self-reported rapid eye movement sleep behaviour disorder symptoms. Changes in thermoregulatory circadian rhythm may be specifically associated with the pathology underlying rapid eye movement sleep behaviour disorder rather than simply that of α-synucleinopathy. These findings implicate thermoregulatory dysfunction as a potential early biomarker for development of rapid eye movement sleep behaviour disorder-associated neurodegeneration, and suggest that subpopulations with differing pathological underpinnings might exist in Parkinson's disease.
TL;DR: It is proposed that during dreams the output of certain pyramidal neurons is mainly driven by input into the apical integration zone (AIZ), and it is suggested that apical drive may also contribute to waking experiences, such as mental imagery.
TL;DR: Translational and clinical studies have reported that disturbances in sleep quality are linked to intestinal inflammation and a heighted systemic immune response and the use of biologics may improve sleep disturbances in patients with IBD.
Abstract: The bidirectional relationship between sleep disorders and inflammatory bowel disease (IBD) has gained considerable attention in recent years. It has been suggested that poor sleep and fatigue are extra-intestinal manifestations of IBD. This review reports recent studies exploring subjective and objective assessments of sleep in the adult IBD population. In ulcerative colitis patients, poor sleep has been independently linked to depression and poorer IBD-related quality of life. Using home polysomnography, IBD patients were shown to have less rapid eye movement sleep and Crohn’s patient had increased lighter sleep. A study utilizing surveys assessing circadian rhythms described circadian misalignment in IBD patients and reported that circadian misalignment in Crohn’s disease was associated with a more aggressive disease phenotype. The use of biologics may improve sleep disturbances in patients with IBD. Translational and clinical studies have reported that disturbances in sleep quality are linked to intestinal inflammation and a heighted systemic immune response. IBD patients appear to have disturbed sleep. Poor sleep is also suggested as a marker for subclinical disease activity. Recent studies have suggested circadian misalignment in IBD patients, and future studies are needed to assess these clinical implications.
TL;DR: The findings suggest that polysomnographic sleep is abnormal in iRBD patients and further studies are needed on underlying mechanisms and associations with neurodegenerative diseases.
TL;DR: It is shown that reactivation occurs in both REM and SWS and that coordination of REM andSWS activation on the same day is associated with rapid learning of a motor skill, and that coordinated reactivation in both sleep states on theSame day, although at different times, is beneficial for skill learning.
Abstract: Neural activity patterns of recent experiences are reactivated during sleep in structures critical for memory storage, including hippocampus and neocortex. This reactivation process is thought to aid memory consolidation. Although synaptic rearrangement dynamics following learning involve an interplay between slow-wave sleep (SWS) and rapid eye movement (REM) sleep, most physiological evidence implicates SWS directly following experience as a preferred window for reactivation. Here, we show that reactivation occurs in both REM and SWS and that coordination of REM and SWS activation on the same day is associated with rapid learning of a motor skill. We performed 6 h recordings from cells in rats' motor cortex as they were trained daily on a skilled reaching task. In addition to SWS following training, reactivation occurred in REM, primarily during the pre-task rest period, and REM and SWS reactivation occurred on the same day in rats that acquired the skill rapidly. Both pre-task REM and post-task SWS activation were coordinated with muscle activity during sleep, suggesting a functional role for reactivation in skill learning. Our results provide the first demonstration that reactivation in REM sleep occurs during motor skill learning and that coordinated reactivation in both sleep states on the same day, although at different times, is beneficial for skill learning. This article is part of the Theo Murphy meeting issue 'Memory reactivation: replaying events past, present and future'.
TL;DR: It is found that a large set of regions in the parietal, frontal, and insular cortices shows increases in 2-4 Hz power during scalp EEG STW, that STW are associated with a strong and widespread increase in high frequencies, and that these slow and fast activities exhibit a high spatiotemporal heterogeneity.
Abstract: Sawtooth waves (STW) are bursts of frontocentral slow oscillations recorded in the scalp electroencephalogram (EEG) during rapid eye movement (REM) sleep. Little is known about their cortical generators and functional significance. Stereo-EEG performed for presurgical epilepsy evaluation offers the unique possibility to study neurophysiology in situ in the human brain. We investigated intracranial correlates of scalp-detected STW in 26 patients (14 women) undergoing combined stereo-EEG/polysomnography. We visually marked STW segments in scalp EEG and selected stereo-EEG channels exhibiting normal activity for intracranial analyses. Channels were grouped in 30 brain regions. The spectral power in each channel and frequency band was computed during STW and non-STW control segments. Ripples (80-250 Hz) were automatically detected during STW and control segments. The spectral power in the different frequency bands and the ripple rates were then compared between STW and control segments in each brain region. An increase in 2-4 Hz power during STW segments was found in all brain regions, except the occipital lobe, with large effect sizes in the parietotemporal junction, the lateral and orbital frontal cortex, the anterior insula, and mesiotemporal structures. A widespread increase in high-frequency activity, including ripples, was observed concomitantly, involving the sensorimotor cortex, associative areas, and limbic structures. This distribution showed a high spatiotemporal heterogeneity. Our results suggest that STW are associated with widely distributed, but locally regulated REM sleep slow oscillations. By driving fast activities, STW may orchestrate synchronized reactivations of multifocal activities, allowing tagging of complex representations necessary for REM sleep-dependent memory consolidation.SIGNIFICANCE STATEMENT Sawtooth waves (STW) present as scalp electroencephalographic (EEG) bursts of slow waves contrasting with the low-voltage fast desynchronized activity of REM sleep. Little is known about their cortical origin and function. Using combined stereo-EEG/polysomnography possible only in the human brain during presurgical epilepsy evaluation, we explored the intracranial correlates of STW. We found that a large set of regions in the parietal, frontal, and insular cortices shows increases in 2-4 Hz power during scalp EEG STW, that STW are associated with a strong and widespread increase in high frequencies, and that these slow and fast activities exhibit a high spatiotemporal heterogeneity. These electrophysiological properties suggest that STW may be involved in cognitive processes during REM sleep.
TL;DR: The results suggest that patients with hyperalgesia and sleep disorders may benefit from operations performed in the morning, as morning operations required a higher dose of anesthetic drugs than did evening operations, which may be related to the circadian rhythm.
Abstract: Objective Postoperative sleep disorders can cause serious adverse effects on postoperative outcomes. The purpose of our study was to compare the effects of the timing of surgery under general anesthesia on intraoperative anesthetic drug requirements, postoperative sleep quality and pain in patients. Materials and methods Eighty-four patients who underwent selective laparoscopic abdominal surgeries under general anesthesia were randomly assigned to the Day Group (8:00-12:00) or the Night Group (18:00-22:00). The portable sleep monitor (PSM) was used to determine sleep quality on the night before surgery (Sleep-preop), the first night after surgery (Sleep POD 1), and the third night after surgery (Sleep POD 3). The visual analog scale (VAS) was used to evaluate postoperative pain scores and the Athens Insomnia Scale (AIS) was used for assessing insomnia symptoms. The total dose of general anesthetics required and adverse effects after surgery were also assessed. Results Compared to Sleep-preop, patients presented with a lower sleep efficiency and a higher AIS score during Sleep POD 1 and Sleep POD 3. Furthermore, the Night Group had a significantly lower proportion of rapid eye movement sleep, stable sleep, and unstable sleep than did the Day Group at Sleep POD 1 and Sleep POD 3. The dosage of propofol and remifentanil required in the Day Group was significantly higher than that in the Night Group. Furthermore, patients in the Day Group had better pain relief, with a lower VAS score at 1, 6, 12, and 24 hours after surgery. The incidences of postoperative nausea and vomiting and dizziness were significantly higher in the Night Group than those in the Day Group. Conclusion Morning operations required a higher dose of anesthetic drugs than did evening operations, which may be related to the circadian rhythm. The degree of postoperative sleep disorders was greater when the operation was performed in the evening than in the morning, which was also associated with increased pain perception and increased incidence of postoperative adverse effects. Thus, our results suggest that patients with hyperalgesia and sleep disorders may benefit from operations performed in the morning.
TL;DR: Results show that outbred rats display significant differences in post-stress sleep and peripheral BDNF identifying these factors as potential markers of resilience and vulnerability prior to traumatic stress.
Abstract: Study objectives To examine the rapid eye movement sleep (REM) response to mild stress as a predictor of the REM response to intense stress and brain-derived neurotrophic factor (BDNF) as a potential biomarker of stress resilience and vulnerability. Methods Outbred Wistar rats were surgically implanted with electrodes for recording electroencephalography (EEG) and electromyogram (EMG) and intraperitoneal Data loggers to record body temperature. Blood was also obtained to measure circulating BDNF. After recovery, rats were exposed to mild stress (novel chamber, NC) and later intense stress (shock training, ST), followed by sleep recording. Subsequently, rats were separated into resilient (Res; n=27) or vulnerable (Vul; n = 15) based on whether or not there was a 50% or greater decrease in REM after ST compared to baseline. We then compared sleep, freezing, and the stress response (stress-induced hyperthermia, SIH) across groups to determine the effects of mild and intense stress to determine if BDNF was predictive of the REM response. Results REM totals in the first 4 hours of sleep after exposure to NC predicted REM responses following ST with resilient animals having higher REM and vulnerable animals having lower REM. Resilient rats had significantly higher baseline peripheral BDNF compared to vulnerable rats. Conclusions These results show that outbred rats display significant differences in post-stress sleep and peripheral BDNF identifying these factors as potential markers of resilience and vulnerability prior to traumatic stress.
TL;DR: It is concluded that both synapse formation or strengthening and elimination or weakening occur across sleep, and sleep-dependent synaptic plasticity plays an important role in neuronal circuit refinement during development and after learning, while sleep disorders may contribute to or exacerbate the development of common neurological diseases.
Abstract: Synaptic plasticity is important for learning and memory. With increasing evidence linking sleep states to changes in synaptic strength, an emerging view is that sleep promotes learning and memory ...
TL;DR: The most frequent sleep problems reported by ET patients were the bad quality of sleep and excessive daytime somnolence, which showed that ET patients showed higher scores in the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale than controls, and lower scores than those of patients diagnosed with Parkinson's disease.
Abstract: Sleep disorders are frequent in patients diagnosed with essential tremor (ET). The present review focuses on sleep disorders and the results of polysomnographic studies performed in patients with ET. For this purpose we performed a systematic review crossing the search term "essential tremor" with "sleep," "sleep disorders," "sleep disturbances" and "polysomnography," and with specific sleep disorders, according to the International Classification of the Sleep Disorders-Third Edition, using the PubMed, EMBASE, MEDLINE, and Web of Science Databases. The most frequent sleep problems reported by patients with ET were the bad quality of sleep and excessive daytime somnolence (the latter could be related to drugs commonly used for the treatment of ET). Probable rapid eye movement sleep behavior disorder, coexistent restless legs syndrome, insomnia, and nocturia were not infrequent complaints, while the presence of other sleep disorders in patients with ET was restricted to anecdotal reports or not described. Meta-analyses of previous reports showed that patients with ET (according to the PRISMA and MOOSE guidelines) showed higher scores in the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale than controls and lower scores than those of patients diagnosed with Parkinson's disease. Studies using polysomnography in patients with ET are scarce and do not permit to establish valid conclusions regarding polysomnographic features in this disorder.
TL;DR: Dream enactment behavior (DEB) is a phenomenon demonstrated in patients with posttraumatic stress disorder, rapid eye movement sleep behavior disorder (RBD), as well as with a more recently described sleep disorder.
Abstract: Dream enactment behavior is a phenomenon demonstrated in patients with post-traumatic stress disorder, rapid eye movement sleep behavior disorder, as well as with a more recently described conditio...
TL;DR: The question of whether individual alpha frequency (IAF) modulates the consolidation of declarative memory across periods of sleep and wake is addressed and the importance of individual factors in the EEG in modulating oscillatory-related memory consolidation and subsequent behavioural outcomes is highlighted.